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Cat. No. ARG36808

IL1R1 Knockout T47D Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Breast (mammary gland)

  • Disease:

    Ductal carcinoma

IL1R1 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population disrupting IL1R1 in the hormone-responsive human T-47D breast cancer cell line. IL1R1 encodes the interleukin-1 receptor type 1, which activates MYD88- and IRAK-dependent NF-??B and MAPK signaling upon ligand binding, driving pro-inflammatory cytokine expression. This knockout model abolishes IL-1 signaling, enabling studies on inflammation-associated breast cancer progression, drug resistance, and therapeutic target validation. Applications include Western blotting for phospho-p65 and phospho-p38, RT-qPCR of IL6 and IL8, NF-??B reporter assays, migration/invasion assays, and proliferation assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    T-47D

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    Metastatic; Pleural effusion

    Gene Name

    IL1R1

    Gene Identifier

    NCBI Gene ID 3554

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 10μg/mL Insulin, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The IL1R1 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human IL1R1 gene in T-47D breast cancer cells. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption, producing a heterogeneous pool of edited cells lacking functional IL-1 receptor type 1. The polyclonal format minimizes clonal artifacts and provides a robust platform for reproducible investigation of IL-1 signaling.

The T-47D cell line is a human breast ductal carcinoma isolated from the pleural effusion of a 54-year-old female with metastatic infiltrating ductal carcinoma. This epithelial cell line naturally expresses estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), making it a well-established model for hormone-responsive breast cancer. Its metastatic origin and epithelial characteristics suit it for studying tumor progression and inflammatory signaling.

IL1R1 encodes the interleukin-1 receptor type 1, which transduces signals from IL1A and IL1B. Upon ligand binding, IL1R1 heterodimerizes with IL1RAP, recruiting MYD88 and activating IRAK4 and IRAK1. These kinases associate with TRAF6, triggering TAK1-dependent activation of the IKK complex and MAPKs, including JNK and p38. This leads to NF-??B and AP-1 translocation, inducing transcription of pro-inflammatory mediators such as IL6, IL8, TNF, and COX2. The pathway is regulated by IL1RN, TOLLIP, and IRAK2, and it controls proliferation, apoptosis, and immune responses.

In T-47D breast cancer cells, IL-1 signaling contributes to inflammation-driven tumor progression, migration, and therapeutic resistance. CRISPR/Cas9-mediated IL1R1 knockout abolishes receptor complex formation, preventing MYD88 and IRAK recruitment and downstream activation of NF-??B and MAPK pathways. Consequently, expression of IL-6, IL-8, and other cytokines is attenuated. This knockout model enables investigation of IL-1-mediated effects on breast cancer proliferation, invasion, and hormone receptor signaling.

These polyclonal knockout cells support diverse research applications, including dissection of IL-1 signaling in breast cancer, inflammation-associated tumor progression, drug resistance studies, and validation of IL-1 pathway inhibitors. Representative assays include Western blotting for phospho-p65 and phospho-p38, RT-qPCR for IL6 and IL8, NF-??B luciferase assays, migration/invasion assays, co-immunoprecipitation of IL1R1-IL1RAP, immunofluorescence, flow cytometry, and MTT proliferation assays. The model is suitable for biomarker discovery and therapeutic target evaluation in an ER+ breast cancer context. For additional information or to inquire about custom configurations, please contact Ascent Research.

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